• MeSH
• Anticoagulants adverse effects   therapeutic use   MeSH
• Hemorrhage chemically induced   MeSH
• Humans MeSH
• Protein C * administration & dosage   adverse effects   therapeutic use   MeSH
• Recombinant Proteins MeSH
• Sepsis drug therapy   complications   MeSH
• Inflammation immunology   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Newspaper Article MeSH

Antiphospholipid syndrome (APS) is a hypercoagulable state accompanied by the presence of heterogeneous antiphospholipid antibodies (aPL), which nonspecifically affect hemostasis by the presence of lupus anticoagulans (LA), anticardiolipin antibodies (aCL), antibodies against β2-glycoprotein-I (anti-β2GPI), but also non-criteria antibodies such as antibodies against β2-glycoprotein-I domain I (anti-DI), anti-phosphatidylserine/prothrombin (anti-PS/PT), anti-annexin V, and many others. The main target of the antibodies is the activated protein C (APC) system, the elimination of which can manifest itself as a thrombotic complication. The aim of this study was to determine the thrombogenicity of antibodies using a modified protein C-activated thrombin generation assay (TGA) on a group of 175 samples suspected of APS. TGA was measured with/without APC and the ratio of both measurements was evaluated (as for APC resistance), where a cut-off was calculated ≤4.5 (90th percentile) using 21 patients with heterozygous factor V Leiden mutation (FV Leiden heterozygous). Our study demonstrates the well-known fact that multiple positivity of different aPLs is a more severe risk for thrombosis than single positivity. Of the single antibody positivity, LA antibodies are the most serious (p value < 0.01), followed by aCL and their subgroup anti-DI (p value < 0.05). Non-criteria antibodies anti-annexin V and anti-PT/PS has a similar frequency occurrence of thrombogenicity as LA antibodies but without statistical significance or anti-β2GPI1 positivity. The modified TGA test can help us identify patients in all groups who are also at risk for recurrent thrombotic and pregnancy complications; thus, long-term prophylactic treatment is appropriate. For this reason, it is proving increasingly beneficial to include the determination antibodies in combination with modified TGA test.

• MeSH
• Antibodies, Antiphospholipid MeSH
• Antiphospholipid Syndrome * complications   MeSH
• Antibodies, Anticardiolipin MeSH
• beta 2-Glycoprotein I MeSH
• Phosphatidylserines MeSH
• Humans MeSH
• Protein C MeSH
• Prothrombin MeSH
• Pregnancy MeSH
• Thrombin MeSH
• Thrombosis * etiology   MeSH
• Check Tag
• Humans MeSH
• Pregnancy MeSH
• Female MeSH
• Publication type
• Journal Article MeSH

• MeSH
• Endothelial Cells * physiology   MeSH
• Blood Coagulation Disorders * etiology   metabolism   MeSH
• Hemorrhage * complications   MeSH
• Humans MeSH
• Oxidation-Reduction MeSH
• Protein C * metabolism   MeSH
• Blood Platelets * physiology   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Review MeSH

Studie ověřuje na vybraných laboratorních parametrech vlastnosti čerstvě zmražené plazmy, skladované v rozmraženém stavu při teplotě 2–6 °C po dobu 5 dnů od rozmražení. Cílem je zhodnocení kvality rozmražené plazmy, připravené k okamžitému podání v příručním krevním skladu na urgentním příjmu nemocnice při řešení stavů masivního krvácení. K měření bylo náhodně vybráno 10 T.U. čerstvě zmražené plazmy (ČZP) pro klinické použití z plné krve o objemu 220 ? 20 ml různých krevních skupin, uchovávaných po dobu nejméně 24 měsíců při teplotě -25 °C a nižší. Odebrané vzorky plazmy po rozmražení byly skladovány při teplotě 2–6 °C po dobu 5 dní. Z ČZP, standardně rozmražené při teplotě 37 °C, byly do dvou hodin odebrány vzorky plazmy k laboratornímu vyšetření a uchování při 2–6 °C po dobu 5 dní. Po tuto dobu byly v pravidelných intervalech měřeny tyto parametry: PT, fibrinogen, AT, APTT, ProC global, Protein C, Protein S, F II, F V, F VII, F VIII, F IX a F X. Měření byla statisticky vyhodnocena neparametrickým Wilcoxonovým párovým testem při srovnání dvou skupin, nebo Friedmanovým testem při srovnání více než dvou párových skupin, p < 0,05 s dvoustranným intervalem spolehlivosti. U většiny sledovaných parametrů byl zaznamenán pozvolný úbytek aktivity v čase. U Proteinu S a F V cca 10% pokles od 3. dne, u serinových proteáz (F II, F VII a F X) cca 20% pokles ke 4. dni. Skokový pokles aktivity o 42,6 % od 2. dne byl pozorován u F VIII, v dalších dnech byla hodnota jeho aktivity již stabilní. Pro klinické použití ČZP vykazují všechny sledované parametry dostatečnou koagulační aktivitu po celou dobu 5denního skladování při teplotě 2–6 °C.

Massive blood transfusion protocol requires having lots of blood products handy as soon as possible. Thawing of FFP costs time, therefore it is desirable to have stock of thawed plasma in hospital emergency room. The aim of study is evaluation of quality of fresh frozen plasma after thawing and during following 5day storage at 2–6°C for use in handy storage. 10 units of FFP various blood groups stored at -25°C were randomly selected and thawed. Samples were kept at 2–6°C for 5 days and tested for various coagulation factors each day during storage. Measured values were analysed using the Wilcoxon matched-pairs test and Friedman Test (nonparametric repeated measures ANOVA). All tests were two-tailed with the level of significance set at 0.05. At most of studied parameters were detected gradual decreases of levels. At Protein S and F V, there was approx. 10% decrease from 3rd day, at serine proteases (F II, F VII and F X) there was approx. 20% decrease up until 4th day. Significant activity decrease of 42.6% from 2nd day was detected at F VIII; in following days, activity was stable. All parameters in thawed FFP stored at 2–6°C for 5 days display sufficient activity for clinical use, but it is preferable that they are used within first 24 hours.

• MeSH
• Antithrombins metabolism   MeSH
• Factor IX metabolism   MeSH
• Factor V metabolism   MeSH
• Factor VII metabolism   MeSH
• Factor VIII metabolism   MeSH
• Factor X metabolism   MeSH
• Fibrinogen metabolism   MeSH
• Blood Coagulation Factors * metabolism   MeSH
• Blood Preservation methods   MeSH
• Plasma * MeSH
• Cryopreservation * MeSH
• Humans MeSH
• Protein C metabolism   MeSH
• Protein S metabolism   MeSH
• Prothrombin metabolism   MeSH
• Prothrombin Time MeSH
• Quality Control MeSH
• Statistics as Topic MeSH
• Blood Coagulation Tests methods   MeSH
• Check Tag
• Humans MeSH

The primary abnormalities that are associated with a risk of venous thrombosis are the deficiencies of protein C. Protein C (PROC), encoded by the PROC gene, acts through its affinity for binding to its transmembrane endothelial cell protein C receptor (EPCR) encoded by the EPCR gene. The objective of the study was to analyze the link between three polymorphisms in the promoter of PROC gene, the polymorphism in the EPCR gene and the occurrence of venous thrombosis. We genotyped 135 individuals - 51 cases with documented venous thrombosis and 84 healthy volunteers without a history of venous thrombosis. The occurrence of the TAA haplotype of PROC gene was significantly more frequent in the controls (N = 48; 57.1%), compared with the patients (N = 18; 35.3%), (P = 0.0206). The healthy individuals were also significantly often carriers of the TAA haplotype and the standard genotype AA of EPCR gene (50 vs. 25.5%) than the patients (P = 0.0066). The frequency of haplotypes CAA and CGT of PROC gene was insignificantly higher in the patients (15.7 and 21.6%, respectively) than in the control group (9.5 and 13.1%). The combination of haplotype CAA/CAA of PROC gene and variant genotype AG of EPCR gene was confirmed with a higher frequency in the group of patients (3.9 vs. 1.2%).This analysis showed that the PROC haplotype associated with a high protein C level (TAA) and the EPCR AA genotype was significantly more frequent in the healthy volunteers (P = 0.0066). Haplotypes associated with a low production of protein C (CAA or CGT) were more frequent in patients with venous thrombosis.

• MeSH
• Antigens, CD genetics   MeSH
• Adult MeSH
• Gene Frequency MeSH
• Genetic Predisposition to Disease MeSH
• Genetic Association Studies MeSH
• Genotyping Techniques MeSH
• Haplotypes MeSH
• Heterozygote MeSH
• Middle Aged MeSH
• Humans MeSH
• Adolescent MeSH
• Polymorphism, Genetic * MeSH
• Prognosis MeSH
• Promoter Regions, Genetic * MeSH
• Protein C genetics   MeSH
• Receptors, Cell Surface genetics   MeSH
• Risk Factors MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Case-Control Studies MeSH
• Venous Thrombosis diagnosis   genetics   pathology   MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Adolescent MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH

• MeSH
• Antibodies, Antiphospholipid analysis   diagnostic use   MeSH
• Antithrombins analysis   diagnostic use   MeSH
• Biomarkers * analysis   blood   MeSH
• Factor VIII analysis   diagnostic use   MeSH
• Homocysteine analysis   diagnostic use   MeSH
• Cardiolipins analysis   diagnostic use   MeSH
• Blood Coagulation Factors analysis   MeSH
• Methylenetetrahydrofolate Reductase (NADPH2) analysis   diagnostic use   genetics   MeSH
• Protein C analysis   diagnostic use   MeSH
• Protein S analysis   diagnostic use   MeSH
• Activated Protein C Resistance diagnosis   blood   MeSH
• Risk Factors MeSH
• Thrombin analysis   biosynthesis   MeSH
• Thrombophilia * diagnosis   etiology   blood   MeSH
• Blood Coagulation Tests methods   instrumentation   MeSH

Hemostáza v organizmu plní svou základní roli, tj. ochranu cévní integrity a udržování normálního průtoku krve. Vedle toho je anatomicky i funkčně propojena s cévním systémem. Klasické koncepce aterosklerózy ukazují klíčovou roli zánětu při vzniku a progresi tohoto onemocnění. Shromažďované údaje ukazují i velmi úzký vztah mezi hemostázou a zánětem, což podtrhuje význam obou systémů v mnoha složitých dějích i onemocněních, včetně procesu aterotrombózy. Bohaté experimentální údaje ukazují, že krevní destičky a koagulační systém jsou důležitými faktory jak aterogeneze, tak i aterotrombózy. Hemostatický systém je významným faktorem v cévním systému a může ovlivnit molekulární i buněčné složení arteriální stěny. Současné pojetí vulnerabilního plátu ukazuje, že opakované mikroruptury plátu, následované subklinickou trombózou, jsou tím kritickým mechanizmem pro růst plátu a jeho vulnerabilitu.

Hemostasis play an essentials role in protecting of vascular integrity and maintaining normal blood flow, and anatomically and functionally is entwined with the vasculature. The classic concept of atherosclerosis assigns a pivotal role to inflammation in the onset and progression of this disease. Accumulating data suggest an intimate cross-talk between hemostasis and inflammation, underscoring the role of both systems in many complex diseases, including atherothrombosis. An experimental data indicate that platelets and the coagulation system are important determinants of both atherogenesis and atherothrombosis. The hemostatic system is well known for its capacity to exert a multitude of actions on the vasculature. The current concept of a vulnerable plaque suggests that repeated plaque microruptures, followed by subclinical thrombosis, are critical for plaque growth and vulnerability.

• Keywords
• hemostatický systém, krevní destičky, antikoagulační terapie,
• MeSH
• Annexin A5 MeSH
• Arteriosclerosis MeSH
• Factor VIII MeSH
• Factor Xa MeSH
• Factor XII MeSH
• Fibrin MeSH
• Fibrinogen MeSH
• Financing, Organized MeSH
• Hemostasis physiology   immunology   MeSH
• Plasminogen Activator Inhibitor 1 MeSH
• Blood Coagulation Factor Inhibitors MeSH
• Blood Coagulation Factors MeSH
• Humans MeSH
• Coagulation Protein Disorders MeSH
• Protein C MeSH
• Protein S MeSH
• Thrombin MeSH
• Blood Platelets MeSH
• Thrombomodulin MeSH
• Thrombosis MeSH
• Inflammation MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH

Venózní tromboembolizmus představuje významný zdravotnický a sociálně ekonomický problém. Ve většině případů se jedná o žilní trombózu v dolní končetině či plicní embolii, méně často o žilní trombózu v jiné lokalizaci, např. v žilách horní končetiny, mozkových splavech, v oblasti splanchniku aj. Incidence onemocnění zůstává v posledních letech stejná, a to přes zlepšení strategie jak primární, tak sekundární profylaxe. Venózní tromboembolizmus má příčinu multifaktoriální a zůstává pro lékaře velkou výzvou, protože se jedná o onemocnění, kterému lze správnými preventivními opatřeními předcházet.

• Keywords
• venózní tromboembolizmu, trombofilní stavy, prevence,
• MeSH
• Antithrombin III MeSH
• Humans MeSH
• Antithrombin III Deficiency MeSH
• Protein C Deficiency MeSH
• Protein S Deficiency MeSH
• Protein C MeSH
• Protein S MeSH
• Activated Protein C Resistance metabolism   MeSH
• Risk Factors MeSH
• Thrombophilia history   genetics   MeSH
• Venous Thromboembolism physiopathology   prevention & control   MeSH
• Check Tag
• Humans MeSH

BACKGROUND: Molecular genetic methods were implemented in the detection of thrombophilic disorders in the 1990's with the discovery of coagulation inhibitors antithrombin III (AT III), protein C (PC) and S (PS). The discovery of the molecular cause of activated protein C (APC) resistance by Bertina in 1994 greatly expanded their utilization. METHODS AND RESULTS: Currently, a broad group of molecular genetic markers with a clearly demonstrated risk of thrombophilia are used--mutation of FV Leiden 506R/Q, mutation of prothrombin (F II) 20210G/A, mutation of methylenetetrahydrofolate reductase (MTHFR) 677C/T in homozygous form, mutation of plasminogen activator inhibitor (PAI-1) 4G/5G, mutations of single coagulation inhibitors as well as a number of polymorphisms with controversial thrombophilic risk such as F XIII Val34Leu, platelet glycoproteins, endothelial protein C receptor and thrombomodulin. Another area utilizing molecular genetic methods is research of the pathophysiology of individual coagulation processes. To date, the greatest advances in regard to APC resistance have been achieved here. Although the molecular cause of APC resistance was clearly demonstrated in the 1990's, its clinical variability has not yet been fully explained. The same is true for the second most widespread mutation, prothrombin gene mutation, where only the latest research has hinted at a possible mechanism of expression of the genetic changes in the actual coagulation process. CONCLUSIONS: The future of molecular genetic methods is in achieving a complex understanding of the pathophysiology of thrombophilia and not only in its utilization as a method for detecting many polymorphisms with a very low risk of thrombosis.

• MeSH
• Antithrombin III genetics   MeSH
• Factor V physiology   genetics   MeSH
• Financing, Organized MeSH
• Blood Coagulation physiology   genetics   MeSH
• Hyperhomocysteinemia genetics   MeSH
• Humans MeSH
• Mutation MeSH
• Protein C genetics   MeSH
• Protein S genetics   MeSH
• Prothrombin genetics   MeSH
• Activated Protein C Resistance genetics   MeSH
• Thrombophilia MeSH
• Thrombosis genetics   blood   physiopathology   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH

Cieľ: Vzťah malignómov k poruchám hemokoagulácie je všeobecne známy. Cieľom práce je analýza poruchy hemokoagulácie pri kolorektálnom malignóme a vyhodnotenie možnosti využitia markerov trombofílie. Materiál a metodika: Autori analyzujú súbor 137 pacientov so zhubným nádorom kólonu a rekta. Porovnávajú výsledky vyšetrení D diméru, plazminogén aktivátor inhibítora (PAI-1), protrombínových fragmentov (F 1+2), Proteínu C s kontrolnou skupinou. Výsledky: Hlavne pri agresívnych formách kolorektálnych malignómov a pokročilých štádiách ochorenia boli preukázané zvýšené hodnoty D diméru a PAI-1. Protrombínové fragmenty 1+2 boli signifikantne vyššie pri dehiscencii anastomózy. Antikoagulačná kapacita proteinu C bola znížená v 6.–7. decéniu a v pokročilejších štádiách ochorenia. Záver: Predoperačné vyšetrenia uvedených markerov trombofílie informujú nielen o riziku trombózy, ale aj o pokročilosti nádorového ochorenia, klinickom štádiu, histopatologickom type nádoru. Preferujú šetrné operačné techniky. Najvyššiu validitu vyšetrenia podáva D dimér a PAI-1.

Aim: Relationship between malignants tumors and damage of hemocoagulation is known. The aim is analyse this damage and evaluate the thrombotic markers. Material and methodics: Authors analyses group of 137 patients with colorectal malignants tumors. They notifyes to relationship between plasmatic preoperative D dimer, PAI-1, F 1+2, Protein C level with controll group. Results: Especially aggressive forms of colorectal tumours have increased levels of D dimer and PAI-1. Protrombin fragments 1+2 were enhanced in the course of anastomotic dehiscence. Protein C level was reduced in 6.–7. decade and in advanced clinical stage. Conclusion: Praeoperative thrombotic markers assays inform about risk of thrombosis and clinical diseases stage. They prefere miniinvasive operations procedures. The maximall validity provides D dimer and PAI-1.

• MeSH
• Adult MeSH
• Fibrin Fibrinogen Degradation Products analysis   MeSH
• Blood Coagulation MeSH
• Colorectal Neoplasms MeSH
• Middle Aged MeSH
• Humans MeSH
• Protein C analysis   MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Thrombophilia diagnosis   complications   MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH